Both active and passive immunization involving Aβ peptides or specific monoclonal antibodies against these peptides have been assessed for the treatment and prevention of AD. Reducing Aβ accumulation by active immunization improves cognitive performance in mice. See, for example, Chen et al., Nature, 408:975-979 (2000); Janus et al. Nature, 408:979-982 (2000). The mechanism by which host-generated antibodies against Aβ clear brain senile plaques is far from being understood. Active immunization experiments use complete Freund's adjuvant, which, by itself, induces leakage of serum proteins, including IgG, through the blood-brain barrier (BBB) 2-3 weeks after injection and cannot be used as an adjuvant in humans. Passive immunization studies are confounded by the integrity of the BBB, which restricts passage of immunoglobulins. The permeability coefficient×surface area (PS) product of IgG has been quantified in rats and found to be very low (0.03-0.1×10−6 mg/sec) and is consistent with a transport mechanism of passive diffusion of fluid-phase endocytosis.